Page 276 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Metabolic Acid-Base Disorders 267

pH i remained greater than 7.00, and hepatic extraction of Racing caused venous lactate concentrations in
lactate (as a percentage of the delivered load) was approxi- greyhounds to increase from 0.57 to 28.93 mEq/L,
mately three times higher than that observed in the hyp- but lactate concentrations returned to 0.53 mEq/L
oxic animals. Hypoxemia reduces hepatic O 2 uptake, and 3 hours after exercise. 119 Arterial pH decreased from
7.365 to 6.997 and returned to 7.372 3 hours after exer-
hepatocyte pH i decreases, presumably as a result of CO 2

accumulation within cells. This study demonstrated that cise, and HCO 3 concentration decreased from 21.1 to
impaired hepatic extraction of lactate is related to 3.1 mEq/L and returned to 20.5 mEq/L 3 hours after
decreased hepatic O 2 uptake and pH i but not to arterial exercise. Plasma potassium concentration does not
pH. During severe hypoxia, increased lactate production increase in response to organic acidosis as it does in acute
6
by gut and muscle and decreased hepatic extraction of lac- mineral acidosis. In the racing greyhounds, there was
tate lead to progressive lactic acidosis. Impaired hepatic no change in plasma potassium concentration despite
extraction of lactate and increased splanchnic production severe lactic acidosis.
also contribute to the lactic acidosis of sepsis in dogs. 48
Cardiac Arrest and Cardiopulmonary Resuscitation
Clinical Features Oxygen delivery to, and CO 2 removal from, tissues are
Lactic acidosis may occur in several clinical settings, dependent on adequate tissue perfusion. Cardiac arrest
especially those associated with poor perfusion and tissue is an extreme example of impaired tissue perfusion. Dur-
hypoxia (e.g., cardiac arrest and cardiopulmonary resusci- ing cardiopulmonary resuscitation (CPR), reduced tissue
tation, shock, left ventricular failure). The clinician perfusion and reduced O 2 delivery cause anaerobic
should strongly consider the possibility of lactic acidosis metabolism and lactic acidosis. In dogs, lactate
in such settings (see Box 10-2). Usually, lactic acidosis concentrations increased linearly during the time
results from accumulation of the L isomer of lactate. between cardiac arrest and the onset of CPR. 38 Lactate
D-Lactic acidosis, characterized by the accumulation of concentrations increased progressively during closed-
the D isomer, is rare but has been reported in human chest CPR in dogs 39 and remained stable but did not
patients with “short-bowel syndrome” in whom gut decrease during 30 minutes of open-chest CPR. 38 In this
bacteria metabolize glucose to D-lactate. Increased model, closed-chest CPR did not provide adequate tissue
concentrations of D-lactate have been observed in cats perfusion and O 2 delivery to halt anaerobic metabolism.
fed propylene glycol 45,46 and in cats with diabetic During CPR, arterial blood gases reflect alveolar-arte-
ketoacidosis, possibly as a result of hepatic ketone metab- rial gas exchange, whereas mixed venous blood gases
47 154
olism. Severe D-lactic acidosis has been documented in reflecttissue acid-basestatusandoxygenation. Respira-
a cat with pancreatic insufficiency, likely as a consequence tory alkalosis develops in arterial blood as a result of
of intestinal bacterial overgrowth. 184 mechanical ventilation, whereas respiratory acidosis
Lactic acidosis should be suspected whenever there is an develops in venous blood because of poor tissue perfusion
unexplained increase in unmeasured anions (i.e., an unex- and impaired transport of accumulated CO 2 to the lungs.
plained increase in the anion gap). Confirmation requires In one study of human patients undergoing CPR, average
measurement of plasma lactate concentration, but this has arterial pH was 7.41, whereas average mixed venous pH
not been performed commonly in small animal practice. was 7.15. 237 Arterial P CO 2 averaged 32 mm Hg and mixed
Care should be taken to prevent vascular stasis when was 74 mm Hg, whereas arterial and venous
venous P CO 2

collecting venous blood for lactate determinations, and HCO 3 concentrations were similar.
blood samples should be centrifuged immediately after Closed-chest CPR, initiated after 6 minutes of cardiac
collection to prevent a spurious increase in lactate concen- arrest, was studied in dogs. 204 Sodium bicarbonate (2
tration related to anaerobic glycolysis by red cells. Lactate mEq/kg) was administered after 20 minutes of cardiac
concentrations in dogs have been reported in many exper- arrest. Administration of NaHCO 3 increased both arterial
*
imental studies. From results of these studies, normal wasapprox-
andvenouspH.BeforeNaHCO 3 ,arterialP CO 2
plasma lactate concentrations in dogs are expected to be imately40mmHg,andwithCPRitdecreasedto20mmHg
less than 2 mEq/L. Control plasma lactate concentrations asaresultofmechanicalventilation.AfterNaHCO 3 ,arterial
in cats were 1.46 mEq/L in one study. 13 In an experimen- P CO 2 increased to 30 mm Hg. Venous P CO 2 was nearly 50
tal model of hemorrhagic shock in dogs, plasma lactate mmHg,anditslowlyincreasedduring30minutesofcardiac
concentration increased from 1.5 to 5.5 mEq/L but did arrest to 60 mm Hg in untreated dogs. Bicarbonate treat-
not completely account for the observed increases in anion ment caused venous P CO 2 to increase transiently to 100
gap and strong ion gap. 30 Other organic anions (especially mm Hg, and it decreased to 70 mm Hg 10 minutes after
acetate and citrate) also contributed to the changes in the NaHCO 3 administration. The pH of CSF was not changed
anion gap and strong ion gap. by NaHCO 3 administration.
The normal arteriovenous pH gradient in dogs is 0.01
*References 37, 39, 82, 86, 94, 110, 113, 114, 119, 121, 128, 133, to 0.04. 8,20,152 Reduced cardiac output increases arterio-
145, 153, 154, 168, 194, 230, 231 venous pH and P CO 2 gradients as a result of arterial